OBJECTIVE: To assess the risk factors, lipid and apolipoprotein profile, hemostasis variables, and polymorphisms of the apolipoprotein AI-CIII gene in early coronary artery disease (CAD). METHODS: Case-control study with 112 patients in each group controlled by sex and age. After clinical evaluation and nutritional instruction, blood samples were collected for biochemical assays and genetic study. RESULTS: Familial history of early CAD (64 vs 39%), arterial hypertension (69 vs 36%), diabetes mellitus (25 vs 3%), and previous smoking (71 vs 46%) were more prevalent in the case group (p<0.001). Hypertension and diabetes were independent risk factors. Early CAD was characterized by higher serum levels of total cholesterol (235 ± 6 vs 209 ± 4 mg/dL), of LDL-c (154 ± 5 vs 135 ± 4 mg/dL), triglycerides (205 ± 12 vs 143 ± 9 mg/dL), and apolipoprotein B (129 ± 3 vs 105 ± 3 mg/dL), and lower serum levels of HDL-c (40 ± 1 vs 46 ± 1 mg/dL) and apolipoprotein AI (134 ± 2 vs 146 ± 2mg/dL) [p<0.01], in addition to an elevation in fibrinogen and D-dimer (p<0.02). The simultaneous presence of the rare alleles of the APO AI-CIII genes in early CAD are associated with hypertriglyceridemia (p=0.03). CONCLUSION: Of the classical risk factors, hypertension and diabetes mellitus were independently associated with early CAD. In addition to an unfavorable lipid profile, an increase in the thrombotic risk was identified in this population. An additive effect of the APO AI-CIII genes was observed in triglyceride levels.

OBJETIVO: Avaliar as alterações obtidas no perfil lipídico de coronariopatas dislipidêmicos, após a adição de colestiramina, em pacientes tratados com inibidores da HMG-CoA redutase, e que não atingiram os valores ideais de LDL-colesterol. MÉTODOS: Vinte coronariopatas (12 submetidos à revascularização do miocárdio, 3 à angioplastia coronária e 5 mantidos sob tratamento clínico), com média de idade de 60,78 anos, que já realizavam dieta hipolipemiante e eram medicados com lovastatina 20mg/dia ou sinvastatina 10mg/dia, receberam também colestiramina na dose de 8 a 16g/dia durante 8 semanas, com o objetivo de reduzir LDL-colesterol para valores inferiores a 100mg/dl. RESULTADOS: Houve significante redução do colesterol total (valor médio inicial 239,52mg/dL e ao final 199,00mg/dL), obtendo-se um decréscimo percentual médio de 16,92%. O valor médio de LDL-colesterol também se reduziu, significantemente, de 172,73mg/dL para 118,26mg/dL, com decréscimo percentual médio de 31,53%. A trigliceridemia média aumentou, ainda dentro da faixa de referência normal, de 145,05mg/dL para 162,00mg/dL, (diferença percentual média de 11,69%). Houve significante aumento da fração HDL-colesterol de um valor médio inicial de 38,00mg/dL para um valor médio final de 48,21mg/dL (diferença média percentual 26,87%). Não houve efeitos adversos que impedissem a continuidade do tratamento. CONCLUSÃO: A associação de colestiramina a doses baixas de vastatinas em pacientes com hipercolesterolemia primária e de alto risco coronário é uma boa opção terapêutica, podendo atingir benefícios sobre o perfil lipídico semelhantes àqueles obtidos quando esses fármacos são utilizados, isoladamente, ou em associação, e em doses mais elevadas.

PURPOSE: To evaluate lipid profile changes associated with cholestyramine addition in hypercholesterolemic patients with established coronary heart disease under treatment with HMG-CoA reductase inihibtors that had not achieved the ideal value of LDL-cholesterol. METHODS: Twenty patients with coronary heart disease, (12 submitted to coronary artery bypass grafts, 3 to coronary angioplasty and 5 maintened under clinical management) with mean age of 60.78 years old, who were under hypolipemic diet and were medicated with lovastatin 20mg/d or simvastatin 10mg/d, received cholestyramine, doses ranging from 8 to 16g/day during 8 weeks, aiming to reduce LDL-cholesterol to values less than 100mg/dL. RESULTS: There was a significant reduction of total cholesterol, from initial mean value of 239.52mg/dL to final mean value of 199.00mg/dL, with a mean reduction of 16.92%. The mean value of LDL-cholesterol was also reduced significantly from 172.73mg/dL to 118.26mg/dL, with a mean reduction of 31.53%. Mean triglyceridemia increased, still within the normal reference values, from 145.05mg/dL to 162.00mg/dL, and the mean difference was 11.69%. There was a significant increase of HDL-cholesterol fraction from an initial mean value of 38.00mg/dL to a final mean value of 48.21mg/dL, mean difference of 26.87%. Side effects were not frequent, and did not interfere in the duration of the study. CONCLUSION: The association of cholestyramine to HMG-CoA reductase inihibtors, both in low doses, in patients with primary hypercholesterolemia and high coronary risk is a good therapeutic option that can reach benefits on the lipid profile similar to those obtained when these drugs are used in association or separately in higher doses.

No protocolo de avaliação clínico-laboratorial de pacientes com acidente vascular cerebral (AVC) aterotrombótico dosamos e analisamos níveis de fibrinogênio plasmático (técnica de Clauss automatizada), para determinar seu possível papel como fator de risco trombogênico em 29 pacientes (20 homens e 9 mulheres) com idades entre 25 a 79 anos (mediana=55); todos tinham tido AVC aterotrombótico. Eles foram classificados em 2 grupos segundo alterações de fluxo nas carótidas: g1 - sem alteração de fluxo (n=19) e g2- com alteração de fluxo (n=10). Resultados- A média das dosagens de fibrinogênio no gl foi de 269 e no g2 de 353 mg/dl. Quarenta e sete por cento dos pacientes do gl e 80% do g2, apresentaram medidas >300 mg/dl. As diferenças obtidas entre os grupos neste estudo foram significantes. Conclusão- Considerando o nível de risco epidemiológico de 300 mg/dl, nossos resultados sugerem que o fibrinogênio é um fator de risco independente para AVC aterotrombótico, especialmente naqueles com alteração de fluxo carotídeo.

We have studied fibrinogen levels (Clauss technique) in atherothrombotic ischemic stroke patients, in order to determine its role as a thombogenic risk factor. Twenty nine patients (20 men and 9 women) between 25 and 79 years old were studied; they all have had a atherothrombotic stroke. They were classified into two groups according to the result of their carotid doppler ultrasonography: g1 - without carotid flow reduction (n=l 9) and g2 - with carotid flow reduction (n=10). The fibrinogen mean value was 269mg/dl in gl and 353 mg/dl in g2. There were 47% of patients in gl and 80% of patients in g2 who presented levels >300 mg/dl. The proportions of the groups were significantly different (p<0,05). Considering the epidemiological value of 300 mg/dl, we conclude that the fibrinogen can be an independent risk factor for ischemic atherothrombotic stroke, specially in those whose carotid flow is reduced.